Project description:This SuperSeries is composed of the following subset Series: GSE4063: Gene expression in skeletal muscle in AMPK gamma3 knock-out mice and wild type littermates GSE4065: Gene expression in skeletal muscle in AMPK gamma3 mutant (R225Q) transgenic mice and wild type littermates. Note: GSE4063 and GSE4065 are not directly comparable. Keywords: SuperSeries Refer to individual Series
Project description:Analysis of AMPK gamma3-dependent transcriptional responses by analyzing global gene expression in the white portion of the gastrocnemius muscle in AMPK gamma3 knock-out mice and corresponding wild type littermates. Keywords: Genetic modification
Project description:Analysis of AMPK gamma3-dependent transcriptional responses by analyzing global gene expression in the white portion of the gastrocnemius muscle in AMPK gamma3 knock-out mice and corresponding wild type littermates.
Project description:Analysis of AMPK gamma3-dependent transcriptional responses by analyzing global gene expression in the white portion of the gastrocnemius muscle in AMPK gamma3 mutant (R225Q) transgenic mice and corresponding wild type littermates. Keywords: Genetic modification
Project description:Analysis of AMPK gamma3-dependent transcriptional responses by analyzing global gene expression in the white portion of the gastrocnemius muscle in AMPK gamma3 mutant (R225Q) transgenic mice and corresponding wild type littermates.
Project description:We show that Mustn1 (Musculoskeletal embryonic nuclear protein 1, also known as Mustang) is highly expressed in skeletal muscle during the early stages of hindlimb reloading. Mustn1 expression is transiently elevated in mouse and human skeletal muscle in response to intense exercise, resistance exercise, or injury. We find that Mustn1 expression is highest in smooth muscle-rich tissues, followed by skeletal muscle fibers. Muscle from heterozygous Mustn1-deficient mice exhibit differences in gene expression related to the extracellular matrix and cell adhesion, compared to wild-type littermates. Mustn1-deficient mice have normal muscle and aorta function and whole-body glucose metabolism. Loss of Mustn1 in vascular smooth muscle cells does not affect their proliferative or migratory functions. We show that Mustn1 can be secreted from smooth muscle cells, and that it is present in arterioles of the muscle microvasculature and in muscle interstitial fluid, in particular during the hindlimb reloading phase. Proteomics analysis of muscle from Mustn1-deficient mice confirms differences in extracellular matrix composition, and female mice display higher collagen content after chemically induced muscle injury compared to wild-type littermates.
Project description:Metabolic dysfunction of skeletal muscle is often prevalent at an early stage in the development of several non-communicable diseases. Here, we investigated the effect of a myokine, secreted protein acidic and rich in cysteine (SPARC), on glucose tolerance in human and mouse skeletal muscles. SPARC knockout mice showed marked decreases in parameters for whole-body glucose metabolism, along with reduced phosphorylation of AMPK and Akt in skeletal muscle tissues compared with wild-type mice. Furthermore, mice injected with SPARC showed improved glucose tolerance concomitant with AMPK activation. Exogenous SPARC treatment accelerated glucose uptake in muscle tissues isolated from wild-type mice but not from AMPKγ3 knockout mice. In muscle cells, SPARC increased glucose uptake concomitant with AMPK activation, mediated by a calcium-dependent signal. Chronic treatment of SPARC restored metabolic functions in diet-induced obese mice. These findings suggest that SPARC improves glucose metabolism via AMPK activation in skeletal muscle, providing mechanistic insights on exercise-induced metabolic benefits and physical inactivity-induced glucose intolerance.